--Study Central Mechanisms of Metabolic Stress and Stem Cell Regulation in Development and Cancer

In our paper published on Nature not too long ago, we found that stem cells and cancer stem cells (CSCs), like hibernating animals, rely primarily on lipid reserves for energy, so that ablation of the Arf1-mediated lipid metabolism results in lipid droplet accumulation and metabolic stress, which promotes CSCs necrosis.

In our papers in submission, we identified the detail molecular mechanisms in both mice and Drosophila. We found that ablation of the Arf1 pathway triggers a chain reaction of multiple cells that coordinately promotes death of stem cells or CSCs. The stressed cells first release danger signals that activate neighboring cells or immune cells, which then feedback to kill the affected cells.

In cancer mice, ablation of the Arf1 pathway can kill two birds with one stone:not only does it kill CSCs, but it also releases danger signals to activate a tumor-specific immune response in which dying CSCs are converted into a therapeutic vaccine to attract and activate immune cells for destroying the bulk tumors and resulting in durable efficacy of the treatment. This is an unique and innovative system. We are using the both mouse and Drosophila genetic models to explore specific molecular mechanisms as well as identify new drug targets for the treatment of cancer and other human diseases. Please view the lab’s website at: https://ccr.cancer.gov/Basic-Research-Laboratory/steven-x-houfor general project information.

Candidates with a strong background in mouse genetics are encouraged to apply.

The minimum annual starting stipend at NCI is ~$56,000 for a new graduate.

The initial appointment is for two years, with an option of renewing for an additional three years.

To apply:

Please send a cover letter, CV including bibliography, and contact information for three references to the following address: